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OBJECTIVES: Our aim is to evaluate the impact of surface ultraviolet radiation intensity on hospital admissions for stroke and to compare the correlation and differences among different subtypes of strokes. MATERIALS AND METHODS: We collected daily data on surface ultraviolet radiation intensity, temperature, air pollution, and hospital admissions for stroke in Harbin from 2015 to 2022. Using a distributed lag non-linear model, we determined the correlation between daily surface ultraviolet radiation intensity and the stroke admission rate. Relative risks (RR) with 95% confidence intervals (CI) and attributable fractions (AF) with 95% CI were calculated based on stroke subtypes, gender, and age groups. RESULTS: A total of 132,952 hospitalized stroke cases (including hemorrhagic and ischemic strokes) were included in the study. We assessed the non-linear effects of ultraviolet intensity on hospitalized patients with ischemic and hemorrhagic strokes. Compared to the maximum morbidity benchmark ultraviolet intensity (19.2 × 10^5 for ischemic stroke and 20.25 for hemorrhagic stroke), over the 0-10 day lag period, the RR for extreme low radiation (1st percentile) was 0.86 (95% CI: 0.77, 0.96), and the RR for extreme high radiation (99th percentile) was 0.86 (95% CI: 0.77, 0.96). In summary, -4.842% (95% CI: -7.721%, -2.167%) and -1.668% (95% CI: -3.061%, -0.33%) of ischemic strokes were attributed to extreme low radiation intensity with a lag of 0 to 10 days and extreme high radiation intensity with a lag of 0 to 5 days, respectively. The reduction in stroke hospitalization rates due to low or high ultraviolet intensity was more pronounced in females and younger individuals compared to males and older individuals. None of the mentioned ultraviolet intensity intensities and lag days had a statistically significant impact on hemorrhagic stroke. CONCLUSIONS: Our study fundamentally suggests that both lower and higher levels of surface ultraviolet radiation intensity in Harbin, China, contribute to a reduced incidence of ischemic stroke, with this effect lasting approximately 10 days. This finding holds significant potential for public health and clinical relevance.
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Non-traumatic intracerebral hemorrhage (ICH) is the most common type of hemorrhagic stroke, most often occurring between the ages of 45 and 60. Hypertension is most often the cause of ICH. Less often, atherosclerosis, blood diseases, inflammatory changes in cerebral vessels, intoxication, vitamin deficiencies, and other reasons cause hemorrhages. Cerebral hemorrhage can occur by diapedesis or as a result of a ruptured vessel. This very dangerous disease is difficult to treat, requires surgery and can lead to disability or death. MicroRNAs (miRNAs) are a class of non-coding RNAs (about 18-22 nucleotides) that are involved in a variety of biological processes including cell differentiation, proliferation, apoptosis, etc., through gene repression. A growing number of studies have demonstrated miRNAs deregulation in various cardiovascular diseases, including ICH. In addition, given that computed tomography (CT) and/or magnetic resonance imaging (MRI) are either not available or do not show clear signs of possible vessel rupture, accurate and reliable analysis of circulating miRNAs in biological fluids can help in early diagnosis for prevention of ICH and prognosis patient outcome after hemorrhage. In this review, we highlight the up-to-date findings on the deregulated miRNAs in ICH, and the potential use of miRNAs in clinical settings, such as therapeutic targets and non-invasive diagnostic/prognostic biomarker tools.
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Background: Glioma is the most common malignant brain tumor of the central nervous system. Despite of the improvement of therapeutic strategy, the prognosis of malignant glioma patients underwent by STUPP strategy is still unexpected. Previous studies have suggested that ticagrelor exerted chemotherapeutic effects by inhibition of epithelial-mesenchymal transition (EMT) in various diseases including tumors. However, whether ticagrelor can exhibit the antitumor efficiency in glioma by affecting the EMT process is still unclear. In this study, we investigated the cancer-fighting role of ticagrelor and demonstrated its chemotherapeutic mechanism in glioma. Materials and methods: The MTT assay was performed to detect the cytotoxicity of ticagrelor in glioma cells. We evaluated the expression of Ki67 in glioma cells by immunofluorescence assay after ticagrelor treatment. We conducted wound healing assay and transwell assay to determine the effects of ticagrelor on the migration and invasion of glioma cells. RNA-seq analysis was conducted to examine potential target genes and alternative signaling pathways for ticagrelor treatment. The expression levels of key EMT -related proteins were examined by Western blot experiment. Results: Ticagrelor inhibited the proliferation, migration and invasion of glioma cells with a favorable toxicity profile in vitro. Ticagrelor downregulated the expression of GTSE1 in glioma cells. RNA-seq analysis explored that GTSE1 acted as the potential target gene for ticagrelor treatment. Upregulation of GTSE1 antagonized the inhibitory effect of ticagrelor on the invasion of glioma and EMT progression by regulation of PI3K/Akt/NF-κB signaling pathway. And ticagrelor also exhibited the similar chemotherapeutic effect of glioma in vivo. Conclusions: Ticagrelor as a potential chemotherapeutic option induced the inhibition of the GTSE1-induced EMT progression by regulation of PI3K/AKT/NF-κB signaling pathway.